Development of new therapeutics for kidney diseases by mitochondia-homig drug

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08064
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Medical pharmacy
• Research Institution: Tohoku University
• Principal Investigator: Suzuki Takehiro 東北大学, 医工学研究科, 特任准教授 (50396438)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ミトコンドリア / 酸化ストレス / ATP / 急性腎障害 / 慢性腎臓病 / 造影剤腎症

Outline of Final Research Achievements

Mitochondrial dysfunction causes various mitochondrial diseases, kidney injuries and cardiomyopathy. Intracellular ATP depletion and the increasing mitochondria-derived reactive oxygen species (mitROS) are considered as major pathophysiologic mechanisms of disease progression in mitochondrial abnormalities. Recently we reported mitochondria homing drug, mitochonic acid-5 (MA-5) increased intracellular ATP, decreased mitochondrial ROS and improved cell survivals of fibroblasts from mitochondrial disease patients by binding mitochondrial protein Mitofilin and promoting oligomelization of ATP synthases MA-5 improved the renal function and tubular cell injuries in murine renal ischemia reperfusion and cisplatin induced nephropathy models. MA-5 also improved mitochondrial respiratory function in kidney and heart of mitochondrial disease model mice (mitomice).

Free Research Field

腎臓内科